Diseased tissue resection at the tissue surface requires precision because tissue surfaces display the shared cell-to-matrix feature of structural stratification. Volumetric or functional over-resection corrupts tissue elements, including intrinsic homeostatic and repair mechanisms, concentrated within the superficial layers at and around these lesions. For many conditions, this imprecision significantly provokes disease progression by eliminating contiguous tissue phenotypes and expanding lesion size toward unsalvageability. The ability to resect diseased tissue precisely, unencumbering contiguous healthy tissue function without iatrogenic impairment of its differentiated phenotype, is a beneficial prerequisite to mitigate the disease burden of tissue-surface based medical conditions. Rather than resection techniques based on imperfect visual-tactile cues designed to unencumber contiguous healthy tissue function, selective targeting of diseased tissue traits protects against the iatrogenic collateral damage of over-resection which can further impair contiguous healthy tissue from retaining and displaying differentiated phenotypes. Early intervention becomes more than an effort to stabilize these lesions into a transient palliative remission indifferent to resection margin accuracy; it becomes a tissue rescue harnessing features unique to tissue surfaces.
Tissue surfaces display a superficial-level healing phenotype because this region is required to interact most intimately with repetitive external tissue-specific stressors. Without these attributes, tissue integrity would be rapidly lost to environmental perturbation. Diseased tissue surfaces manifest as forces or processes overload the tissue's capacity to maintain integrity. Untreated, this tissue burden can ultimately lead to symptoms of disease progression. While the topographic loss of water-structured surface barrier regimes such as stratified zones of structured fluid organized in a potentiometric manner of charge separated areas and the collagen failure of backup layered cleavage planes occur during physiologic loading, these lesions are generally self-repaired by intrinsic tissue assembly mechanisms. The factors by which in vivo self-repair becomes insufficient are complex and tissue-specific. Lesions that remain reversible require targeted resection of the diseased tissue that serves as a biophysical irritant impeding regional tissue organization and assembly. This irritant changes the tissue-surface microenvironment, impeding reconstitution of damaged surface barrier regimes and altering chemo-mechano-transductive gene expression in contiguous tissue, progressively advancing reversible lesions toward failed differentiated homeostatic resistance capacity and an unsalvageable state characterized by non-reversible phenotypic alterations.
Early surgical intervention may be viewed as a tissue rescue, allowing articular cartilage to continue displaying biologic responses appropriate to its function, rather than converting to a tissue ultimately governed by the degenerative material property responses of matrix failure. Early intervention may positively impact the late changes and reduce disease burden of damaged articular cartilage.
A goal of early surgical intervention for treatment of articular cartilage damage is to stabilize lesions as a means to decrease symptoms and disease progression. Lesion stabilization remains a necessary prerequisite toward articular cartilage tissue preservation since removing the irritant of damaged tissue and creating a residually healthy lesion site remain required substrates for permitting or inducing effective in situ healing responses.
For articular cartilage lesion stabilization, thermal and plasma radiofrequency ablation devices originally appeared to be more efficacious than mechanical shavers by exhibiting a smaller time-zero collateral injury footprint. However, because matrix corruption and chondrocyte depletion within contiguous healthy tissue occur commensurate with, and often significantly expand following, volumetric tissue removal, this technology did not become widely adopted as it is understandable that such damage can impair or inhibit in situ healing responses as well as contribute to disease progression by enlarging lesion size. Despite optimizing ablation device performance, this collateral tissue damage transgresses tissue zonal boundaries wherein the depth of necrosis in non-targeted tissue remains larger than native Superficial Zone thickness. Consequently, the functional properties and vital healing phenotype of the Superficial Zone is always effectively eliminated. These collateral wounds originate because ablation technology, like mechanical shavers, cannot distinguish between damaged and undamaged tissue.
Utilizing direct electrode-to-tissue interfaces known in the art indiscriminately deposits current into tissue which causes surface entry wounds and subsurface necrosis through resistive tissue heating and tissue electrolysis; and, because of its high water content, articular cartilage is inherently at risk for efficiently pooling electrothermal energy to a detrimental level. Some have advocated manually positioning the active electrode away from healthy tissue to target diseased tissue. However, this technique significantly increases the amount of current required to overcome the effects that the fluid-flow and convective forces present during surgical application exert on exposed device electrodes. Others have offered that intentional current-based damage serves as a barrier to additional current deposition without demonstrating damage efficacy. Still others utilize current to create ionizing electromagnetic radiation associated with high temperature plasma formation, which has raised further concerns regarding iatrogenic chondrocyte DNA fragmentation and nuclear condensation. Both can induce apoptosis, cellular senescence, decreased progenitor cell populations, diminished cellular differentiation potential, and altered extracellular matrix structure and production. Additional effects of ionizing electromagnetic radiation on chondrocyte behavior important for in situ healing responses remain a cause for concern.
The disturbance of surface-confined nanoscale assemblies in biologic tissue brought about by normative interfacial environments during therapeutic intervention has received very little attention despite the significant role these assemblies play in maintaining tissue integrity against perturbation and pathologic solutes. While much has been written about the interfacial nuances of tissue surfaces for over 125 years, the emergence of tissue rescue surgical procedures has generated a renewed interest in surface-confined assemblies because these assemblies are enrolled to produce a healthy lesion site devoid of damaged tissue as a means to unencumber innate and facilitative wound healing. Although becoming increasingly more delineated in various tissue types, surface-confined assemblies remain complex and difficult to study, even without imposing iatrogenic disturbances and non-equilibria treatment conditions. Treatment venues that utilize endoscopic surgical access procedures to care for normally juxtaposed tissue surfaces necessarily involve ambient media replacement and mechanical loading alterations, both of which disturb surface-confined assembly behavior despite attempts to simulate in vivo conditions.
Endoscopic replacement media such as saline solutions were originally intended to aid surgical visualization as native media do not display either consistent or suitable optical properties. Commensurate with this effort were attempts to limit detrimental effects upon interstitial matrices and resident cells, followed by the consideration of medical device performance within replacement media, both without significant deference to surface-confined assembly effects or their reversibility (damaged tissue removal was an obvious entry-level procedural advance once endoscopic access and visualization was made possible. For articular cartilage, early efforts like powered mechanical shavers and electrosurgical (thermal or plasma) ablation devices were based on imperfect visual-tactile cues rather than upon tissue traits that relate the practitioner's ability to distinguish diseased tissue from normal as correlated to conditions that contribute to disease burden. Tissue rescue treatments are designed to unencumber contiguous healthy tissue function by selectively targeting diseased tissue traits to protect against the iatrogenic collateral).
Media replacement eliminates native fluid lubricants required to accommodate physiologic movement between normally juxtaposed tissue surfaces; consequently, interfacial behaviors associated with hydrodynamic fluid film dissolution-depletion occur so that surface asperities are no longer contained within the thickness of native fluid lubricant pools. Such native fluid film starvation is induced by the lower media viscosity associated with optical improvement and the mechanical unloading that occurs by eliminating the normal contact between tissue surfaces. Because pressure build up in native viscous lubricants is inhibited during endoscopy, interruption of other interfacial regimes like squeeze film, interstitial biphasic, mixed-mode, or versions of elastohydrodynamic fluid film mechanisms can inevitably occur (replacement media pressurization within a constrained endoscopic cavity can produce significant hydrostatic forces; and in certain settings, residual lubricant entrapment may occur. Further, the role of hydrodynamic fluid film regimes during endoscopy for porous tissue surfaces like articular cartilage remains to be fully clarified, including the effects porosity may exert upon wettability). These conditions favor the expression of boundary lubrication regimes whereat loading is carried by the surface asperities in a contact area rather than by a fluid film lubricant and at which surface chemistry dominates working properties.
Because the differential mechanical load that tissue surfaces experience during endoscopy is primarily due to surgical device contact, this situation is ideally suited for the treatment of abnormal surface asperities as relative to boundary conditions. Conversely, the disturbances provoked by fluid film starvation and absent hydrodynamic pressure regimes during endoscopy that express boundary conditions constitutes a tissue vulnerability that has been largely unrecognized as an etiologic factor associated with iatrogenic damage that further impairs wound healing, expands lesion size, and contributes to disease burden.
Partial-thickness damaged tissue surfaces at locations requiring relative motion characteristically exhibit abnormal surface asperities and the related absence of surface-confined assemblies associated with boundary lubrication regimes, features that serve as an effective nanoscale trait-targeting substrate for tissue rescue procedures which mimic biologic wound healing behaviors.
Note that the following discussion refers to a number of publications by author(s) and year of publication, and that due to recent publication dates certain publications are not to be considered as prior art vis-a-vis embodiments of the present invention. Discussion of such publications herein is given for more complete background and is not to be construed as an admission that such publications are prior art for patentability determination purposes.